Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex

Vincent Géli, Michael Lisby*

*Corresponding author af dette arbejde
25 Citationer (Scopus)

Abstract

The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of "difficult to repair" lesions such as double-strand breaks without a repair template and eroded telomeres in telomerase-deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure-forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC-facilitated repair.

OriginalsprogEngelsk
TidsskriftBioEssays
Vol/bind37
Udgave nummer12
Sider (fra-til)1287-1292
Antal sider6
ISSN0265-9247
DOI
StatusUdgivet - 2015

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